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Differential Effects of Insulin on Choline Acetyltransferase and Glutamic Acid Decarboxylase Activities in Neuron‐Rich Striatal Cultures
Author(s) -
Brass B. J.,
ner D.,
Barrett J. N.
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb09387.x
Subject(s) - choline acetyltransferase , insulin , medicine , endocrinology , glutamate decarboxylase , cholinergic neuron , cholinergic , biology , nerve growth factor , chemistry , biochemistry , receptor , enzyme
We studied the effects of insulin, nerve growth factor (NGF), and tetrodotoxin (TTX) on cellular metabolism and the activity of glutamic acid decarboxylase (GAD) and choline acetyltransferase (ChAT) in neuron‐rich cultures prepared from embryonic day 15 rat striatum. Insulin (5 μg/ml) increased glucose utilization, protein synthesis, and GAD activity in cultures plated over a range of cell densities (2,800‐8,400 cells/mm2). TTX reduced GAD activity; NGF had no effect on GAD activity. Insulin treatment reversibly reduced ChAT activity in cultures plated at densities of >4,000 cells/mm2, and the extent of this reduction increased with increasing cell density. The number of acetylcholinesterase‐positive neurons was not reduced by insulin, suggesting that insulin acts by down‐regulating ChAT rather than by killing cholinergic neurons. Insulin‐like growth factor‐1 (IGF‐1) reduced ChAT activity at concentrations 10‐fold lower than insulin, suggesting that insulin's effect on ChAT may involve the IGF‐1 receptor. NGF increased ChAT activity; TTX had no effect on ChAT activity. These results suggest that striatal cholinergic and GABAergic neurons are subject to differential trophic control.